The present invention, in some embodiments thereof, relates to a cardiac valve support, more particularly, but not exclusively, to a cardiac valve support for a prosthesis for a cardiac valve, and more particularly, but not exclusively, to a cardiac valve prosthesis.
The term “frame” is used throughout the present specification and claims to mean a support for a cardiac valve. In some embodiments the cardiac valve is optionally a fabric designed to act as a cardiac valve, attached to the frame. In some embodiments the cardiac valve is optionally a plastic and/or synthetic and/or metal valve.
The mitral valve and tricuspid valve are unidirectional heart valves which separate the left and right atria respectively, from corresponding heart ventricles. These valves have a distinct anatomical and physiological structure, having two (mitral) or three (tricuspid) sail-like leaflets connected to a sub-valvular mechanism of strings (chordae tendinae) and papillary muscles forming a part of the heart's ventricular shape, function and size.
The heart has four chambers: the right and left atria, and the right and left ventricles. The atria receive blood and then pump it into the ventricles, which then pump it out into the body.
Synchronous pumping actions of the left and right sides of the heart constitute the cardiac cycle. The cycle begins with a period of ventricular relaxation, called ventricular diastole. The cycle ends with a period of ventricular contraction, called ventricular systole.
The heart has four valves which are supposed to ensure that blood does not flow in the wrong direction during the cardiac cycle; that is, to ensure that the blood does not back flow from the ventricles into the corresponding atria, or back flow from the arteries into the corresponding ventricles. The valve between the left atrium and the left ventricle is the mitral valve. The valve between the right atrium and the right ventricle is the tricuspid valve. The pulmonary valve is at the opening of the pulmonary artery. The aortic valve is at the opening of the aorta.
The opening and closing of heart valves occur primarily as a result of pressure differences. For example, the opening and closing of the mitral valve occurs as a result of the pressure differences between the left atrium and the left ventricle. During ventricular diastole, when ventricles are relaxed, the venous return of blood from the pulmonary veins into the left atrium causes the pressure in the atrium to exceed that in the ventricle. As a result, the mitral valve opens, allowing blood to enter the ventricle. As the ventricle contracts during ventricular systole, intra-ventricular pressure rises above the pressure in the atrium and pushes the mitral valve shut.
As noted above, these valves feature a plurality of leaflets connected to chordae tendinae and papillary muscles, which allow the leaflets to resist the high pressure developed during contractions (pumping) of the left and right ventricles. In a healthy heart, the chordae become taut, preventing the leaflets from being forced into the left or right atria and inverted. Prolapse is a term used to describe a condition wherein coaptation edges of each leaflet initially may coapt and close, but then the leaflets rise higher, the edges separate, and the valve leaks. This is normally prevented by a contraction of the papillary muscles and by the normal length of the chordae. Contraction of the papillary muscles is usually simultaneous with the contraction of the ventricle and serves to keep healthy valve leaflets tightly shut at peak contraction pressures exerted by the ventricle.
Valve malfunction can result from the chordae becoming stretched, and in some cases tearing. When a chord tears, the result is a flailed leaflet. Also, a normally structured valve may not function properly because of an enlargement of the valve annulus pulling the leaflets apart. This condition is referred to as a dilation of the annulus and generally results from heart muscle failure. In addition, the valve may be defective at birth or because of an acquired disease, usually infectious or inflammatory.
Diseases of the valves can cause either narrowing (stenosis) or dilatation (regurgitation, insufficiency) of the valve, or a combination of those. Surgical treatment for repair or replacement of the valves typically includes an open-heart procedure, extracorporeal circulation and, if replaced, a complete or partial resection of the diseased valve.
Additional background art includes:
U.S. Pat. No. 7,381,220 to Macoviak et al;
U.S. Pat. No. 8,579,964 to Lane et al;
US published patent application number 2014/0052237 of Lane et al;
US published patent application number 2010/0280606 of Naor;
US published patent application 2010/010017 of Letac et al;
US published patent application number 2007/0270943 of Solem et al;
US published patent application number 2007/0185571 of Kapadia et al;
US published patent application number 2007/0156233 of Kapadia et al;
US published patent application number 2006/0058871 of Zakay et al;
US Published Patent Application 2004/0127981A1 of Randert et al;
US published patent application number 2003/0199975 of Gabbay;
PCT patent application number IL2014/050414 of Naor;
PCT published patent application WO2013/076724 of Vaturi;
PCT published patent application WO2011/137531 of Lane et al;
PCT published patent application number WO 2011/069048 of Chau et al;
PCT published patent application number WO 2011/106544 of Tuval et al;
PCT published patent application number WO 2011/137531 of Lane et al;
PCT Published Patent Application WO2010/106438 of Naor et al; and
PCT published patent application number WO 2005/027797 of Ersin.
PCT published patent application number WO 2004/089250 of Realyvasquez et al.
PCT published patent application number WO 2004/030568 of Macoviak et al.
The disclosures of all references mentioned above and throughout the present specification, as well as the disclosures of all references mentioned in those references, are hereby incorporated herein by reference.